SLU-PP-332
Synthetic Pan-ERR Agonist · Exercise Mimetic & Metabolic Modulator
Groundbreaking synthetic compound from Saint Louis University functioning as pan-estrogen-related receptor agonist with preferential ERRα activity. Activates metabolic pathways engaged during physical exercise without physical activity requirement.
Overview
Groundbreaking synthetic compound from Saint Louis University functioning as pan-estrogen-related receptor agonist with preferential ERRα activity. Activates metabolic pathways engaged during physical exercise without physical activity requirement.
Binds and activates ERRα/β/γ which regulate energy metabolism gene expression. Upregulates PGC-1α (mitochondrial biogenesis master regulator), activates AMPK pathway, increases mitochondrial density to 1.8-fold, enhances oxidative phosphorylation and ATP production.
Research indications
What the compound has been studied for, grouped by body system. Effect size is the reported magnitude where it was measured — not a recommendation.
12% body weight reduction in 28 days without appetite suppression. Fat mass gain <0.5g vs ~5g controls.
Significantly improved glucose tolerance in obese mice with lower fasting glucose and insulin levels.
Increases resting energy expenditure by 25% for fatty acid oxidation within 2 hours.
Reduced hepatic steatosis, decreased hepatic triglycerides, and enhanced hepatic fatty acid oxidation.
70% increase in running time and 45% increase in running distance in preclinical models.
Increased type IIa oxidative skeletal muscle fibers with enhanced oxidative capacity.
Improved ejection fraction in heart failure models with reduced cardiac fibrosis.
First compound to reverse age-related mitochondrial dysfunction in 21-month-old mice.
Reversed age-related albuminuria increase and prevented podocyte loss in elderly mice.
A large effect in a weak study and a small effect in a strong one are different things. Effect size is never evidence of use in people.
- Class
- Synthetic ERR agonist
- Molecular weight
- 290.32 Da
- Typical dose
- NO HUMAN DOSE ESTABLISHED (animal studies: 50 mg/kg IP)
- Frequency
- Research only - not approved for human use
- Cycle length
- No human protocols established
- Storage
- 2-8°C refrigerated for research use
Molecular data
- Type
- Synthetic ERR agonist
- Molecular weight
- 290.32 Da
Dosing reference
Doses reported in the literature and by suppliers. These are a record of what has been used in research — reference, never instruction.
| Context | Route | Amount | Frequency |
|---|---|---|---|
| Standard Metabolic Protocol | Intraperitoneal injection (IP) | 50 mg/kg (animal dosing) | Twice daily |
| Acute Exercise Enhancement | Intraperitoneal injection (IP) | 50 mg/kg (animal dosing) | Single dose 1 hour pre-exercise |
| Extended Treatment | Intraperitoneal injection (IP) | 50 mg/kg (animal dosing) | Twice daily for 4-8 weeks |
Interactions
Both affect mitochondrial function and AMPK pathways - may have additive metabolic effects. Monitor blood glucose closely.
Enhanced insulin sensitivity may require significant dose reduction to prevent hypoglycemia.
Different mechanisms affecting weight loss and metabolism - combination could have additive effects.
Combining GLP-1 and ERR agonism may enhance metabolic effects - monitor weight loss rate closely.
Distinct mechanisms (ERR agonism vs NNMT inhibition) likely complementary without known interactions.
Complementary mitochondrial pathways - SLU-PP-332 increases biogenesis while NAD+ supports energy production.
GH optimization may complement metabolic enhancement for body composition without known interactions.
May preserve lean muscle during SLU-PP-332-induced fat loss through GH pathway.
Quality checklist
- ✓Legitimate research supplier with Certificate of Analysis
- ✓From reputable chemical suppliers (Cayman Chemical, Sigma-Aldrich)
- ✓Proper labeling as 'Research Use Only'
- ✓Batch numbers and purity data (typically >98%)
- !Research chemical only - NOT FOR HUMAN USE
- !NOT FDA approved - no human clinical trials
- !Available only for legitimate research through licensed suppliers
- ×Any product marketed for human consumption is illegal
- ×Unknown purity or contamination without lab testing
- ×Lack of proper HPLC or mass spectrometry verification
- ×Products without 'Research Use Only' labeling
What to expect
Safety
- Animal studies show favorable safety with no severe effects at therapeutic doses
- Well-tolerated in rodents and canines
- No liver, kidney, or cardiac toxicity documented
- No lean mass loss
- Does not suppress hormones or act as stimulant
- Minor plasma cholesterol and liver enzyme changes in some studies
- Severe hypoglycemia (especially with diabetes medications)
- Any cardiovascular symptoms (chest pain, palpitations, shortness of breath)
- Signs of liver dysfunction (jaundice, dark urine, severe abdominal pain)
- Kidney problems (reduced urination, swelling, severe back pain)
- Severe headaches or neurological symptoms
- Allergic reactions (rash, hives, difficulty breathing, swelling)
- NOT FOR HUMAN USE - no approved human dose
- No human clinical trials conducted
- Potential interaction with diabetes medications
FAQ
Is SLU-PP-332 an actual exercise substitute, or does it just feel like you worked out?
SLU-PP-332 activates the same metabolic pathways exercise does (mitochondrial biogenesis, PGC-1α upregulation, AMPK activation), but it's not a complete substitute. It increases endurance 70% and reduces weight 12% without exercise, but it doesn't build muscles or improve cardiovascular fitness like real training does. Think of it as metabolic enhancement, not exercise replacement.
Why does SLU-PP-332 work so much faster than training (12% weight loss in 28 days)?
Training requires weeks to upregulate mitochondrial genes; SLU-PP-332 activates them within hours. In mouse studies, energy expenditure increased 25% within 2 hours, creating sustained fat oxidation and rapid weight loss. This bypass of normal training adaptation pathways explains the speed, though long-term human data doesn't exist.
Could SLU-PP-332 cause liver damage if used long-term?
The file flags SLU-PP-332 as potentially hepatotoxic. However, animal studies showed no liver damage at therapeutic doses. The flag exists because long-term human safety is unknown. If used experimentally, liver function tests (ALT, AST, bilirubin) should be monitored regularly.
Is there an oral version of SLU-PP-332 in development?
Yes. SLU-PP-915 (a distinct oral bioavailable ERR pan-agonist) shows similar efficacy to SLU-PP-332 when given orally. A 2025 study found it enhanced aerobic performance as effectively as the injectable form. This represents major progress toward clinical translation, though human trials haven't started.
References
- 1Synthetic ERRα/β/γ Agonist Induces an ERRα-Dependent Acute Aerobic Exercise Response and Enhances Exercise CapacityBillon C, Sitaula S, Banerjee S, Welch R, Elgendy B, Hegazy L, Oh TG, Kazantzis M, Chatterjee A, Chrivia J et al. · ACS Chemical Biology · 2023
Multiple mouse models, 50 mg/kg IP: 70% increase in running time, 45% increase in running distance, increased type IIa oxidative muscle fibers. SLU-PP-332 is a synthetic ERR pan agonist with highest potency for ERRα.
animalPubMed 36988910 ↗ - 2Estrogen-Related Receptor Agonism Reverses Mitochondrial Dysfunction and Inflammation in the Aging KidneyWang XX, Myakala K, Libby AE, Krawczyk E, Panov J, Jones BA, Bhasin K, Shults N, Qi Y, Krausz KW et al. · American Journal of Pathology · 2023
21-month-old mice, 8-week treatment with SLU-PP-332: Reversed age-related increases in albuminuria, podocyte loss, mitochondrial dysfunction, and inflammatory cytokines.
animalPubMed 37717940 ↗ - 3A Synthetic ERR Agonist Alleviates Metabolic SyndromeBillon C, Schoepke E, Avdagic A, Chatterjee A, Butler AA, Elgendy B, Walker JK, Burris TP · Journal of Pharmacology and Experimental Therapeutics · 2024
Diet-induced obese mice, 50 mg/kg IP twice daily, 28 days: 12% body weight loss, 25% fatty acid oxidation increase, improved glucose tolerance, reduced hepatic steatosis. SLU-PP-332 mimics exercise-induced metabolic benefits.
animalPubMed 37739806 ↗ - 4Novel Pan-ERR Agonists Ameliorate Heart Failure Through Enhancing Cardiac Fatty Acid Metabolism and Mitochondrial FunctionXu W, Billon C, Li H, Wilderman A, Qi L, Graves A, Rideb JRDC, Zhao Y, Hayes M, Yu K et al. · Circulation · 2024
Both SLU-PP-332 and SLU-PP-915 significantly improved ejection fraction, ameliorated fibrosis, and increased survival in pressure overload-induced heart failure without affecting cardiac hypertrophy. Transcriptionally activated fatty acid metabolism and mitochondrial function genes.
reviewPubMed 37961903 ↗